Hata Tissa R, Gallo Richard L
Division of Dermatology, University of California San Diego, San Diego, CA, USA.
Semin Cutan Med Surg. 2008 Jun;27(2):144-50. doi: 10.1016/j.sder.2008.04.002.
The innate immune system evolved more than 2 billion years ago to first recognize pathogens then eradicate them. Several distinct defects in this ancient but rapidly responsive element of human immune defense account for the increased incidence of skin infections in atopics. These defects include abnormalities in the physical barrier of the epidermis, alterations in microbial pattern recognition receptors such as toll receptors and nucleotide binding oligomerization domains, and a diminished capacity to increase the expression of antimicrobial peptides during inflammation. Several antimicrobial peptides are affected including; cathelicidin, HBD-2, and HBD-3, which are lower in lesional skin of atopics compared with other inflammatory skin diseases, and dermcidin, which is decreased in sweat. Other defects in the immune defense barrier of atopics include a relative deficiency in plasmacytoid dendritic cells. In the future, understanding the cause of these defects may allow therapeutic intervention to reduce the incidence of infection in atopic individuals and potentially decrease the severity of this disorder.
先天免疫系统在二十多亿年前就已进化形成，它首先识别病原体，然后将其根除。人类免疫防御系统中这个古老但反应迅速的部分存在一些明显缺陷，这导致了特应性个体皮肤感染发病率的增加。这些缺陷包括表皮物理屏障异常、微生物模式识别受体（如Toll样受体和核苷酸结合寡聚化结构域）改变，以及炎症期间抗菌肽表达增加能力的减弱。几种抗菌肽受到影响，包括：与其他炎症性皮肤病相比，特应性个体皮损部位的cathelicidin、HBD - 2和HBD - 3含量较低，而汗液中的dermcidin含量减少。特应性个体免疫防御屏障的其他缺陷包括浆细胞样树突状细胞相对缺乏。未来，了解这些缺陷的原因可能有助于进行治疗干预，以降低特应性个体的感染发生率，并有可能减轻这种疾病的严重程度。
